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NR 601: Week 6 Quiz Review of Week 5 Diabetes ·

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NR 601: Week 6 Quiz Review Week 5 Diabetes · ADA screening recommendations: when to screen to repeat screens based on findings Recommendations Screening for type 2 diabetes with an informal assessmen... t of risk factors or validated tools should be considered in asymptomatic adults. B Testing for type 2 diabetes in asymptomatic people should be considered in adults of any age who are over- weight or obese (BMI >25 kg/m2 or $23 kg/m2 in Asian Americans) and who have one or more additional risk factors for diabetes. B For all people, testing should be- gin at age 45 years. B If tests are normal, repeat testing carried out at a minimum of 3-year intervals is reasonable. C To test for type 2 diabetes, fasting plasma glucose, 2-h plasma glucose after 75-g oral glucose tolerance test, and A1C are equally appropriate. B In patients with diabetes, identify and treat other cardiovascular disease risk factors. Updated recommendations emphasize that testing for prediabetes and type 2 diabetes should be considered in children and adolescents younger than 18 years of age who are overweight or obese (BMI >85th percentile for age and sex, weight for height >85th percentile, or weight >120% of ideal for height), and have one or more additional risk factors for diabetes such as (1) maternal history of diabetes or gestational diabetes during the child’s gestation; (2) family history of type 2 diabetes in first- or seconddegree relative; (3) race/ethnicity (Native American, African American, Latino, Asian American, Pacific Islander; and/or (4) signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, hypertension, dyslipidemia, polycystic ovary syndrome, or smallDIAGNOSTIC TESTS FOR DIABETES Diabetes may be diagnosed based on plasma glucose criteria, either the fasting plasma glucose (FPG) or the 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT) or A1C criteria (1,6) (Table 2.2). FPG, 2-h PG after 75-g OGTT, and A1C are equally appropriate for diagnostic testing. It should be noted that the tests do not necessarily detect diabetes in the same individuals. The efficacy of interventions for primary prevention of type 2 diabetes (7,8) has primarily been demonstrated among individuals with impaired glucose tolerance (IGT), not for individuals with isolated impaired fasting glucose (IFG) or for those with prediabetes defined by A1C criteria. The same tests may be used to screen for and diagnose diabetes and to detect individuals with prediabetes. Diabetes may be identified anywhere along the spectrum of clinical scenarios: in seemingly low-risk individuals who happen to have glucose testing, in individuals tested based on diabetes risk assessment, and in symptomatic patients. Fasting and 2-Hour Plasma Glucose The FPG and 2-h PG may be used to diagnose diabetes (Table 2.2). The concordance between the FPG and 2-h PG tests is imperfect, as is the concordance be- tween A1C and either glucose-based test. Numerous studies have confirmed that, compared with FPG and A1C cut points, the 2-h PG value diagnoses more people with diabetes. A1C The A1C test should be performed using a method that is certified by the NGSP (www.ngsp.org) and standardized or traceable to the Diabetes Control and Complications Trial (DCCT) reference as- say.Although point-of-care A1C assays may be NGSP certified, proficiency testing is not mandated for performing the test, so use of point-of-care assays for diagnostic purposes is not recommended but may be considered in the future if proficiency testing is performed and documented. The A1C has several advantages com- pared with the FPG and OGTT, including greater convenience (fasting not required), greater preanalytical stability, and less day-to-day perturbations during stress and illness. However, these advantages may be offset by the lower sensitivity of A1C at the designated cut point, greater cost, limited availability of A1C testing in certain regions of the developing world, and the imperfect correlation between A1C and average glucose in certain individuals. National Health and Nutrition Examination Survey (NHANES) data indicate that an A1C cut point of $6.5% (48 mmol/mol) identifies one-third fewer cases of undiagnosed diabetes than a fasting glucose cut point of $126 mg/dL (7.0 mmol/L) (9). When using A1C to diagnose diabetes, it is important to recognize that A1C is an indirect measure of average blood glucose levels and to take other factors into consideration that may impact hemoglobin glycation independently of glycemia including age, race/ethnicity, and anemia/ hemoglobinopathies. Confirming the Diagnosis Unless there is a clear clinical diagnosis (e.g., patient in a hyperglycemic crisis or with classic symptoms of hyperglycemia and a random plasma glucose $200 mg/dL [11.1 mmol/L]), a second test is required for confirmation. It is recommended that the same test be repeated without delay using a new blood sample for confirmation because there will be a greater likelihood of concurrence. For ex- ample, if the A1C is 7.0% (53 mmol/mol) and a repeat result is 6.8% (51 mmol/mol), the diagnosis of diabetes is confirmed. If two different tests (such as A1C and FPG) are both above the diagnostic threshold, this also confirms the diagnosis. On the other hand, if a patient has discordant results from two different tests, then the test result that is above the diagnostic cut point should be repeated. The diagnosis is made on the basis of the confirmed test. For example, if a patient meets the diabetes criterion of the A1C (two results $6.5% [48 mmol/mol]) but not FPG (,126 mg/dL [7.0 mmol/L]), that person should nevertheless be considered to have diabetes. Since all the tests have preanalytic and analytic variability, it is possible that an abnormal result (i.e., above the diagnostic threshold), when repeated, will produce a value below the diagnostic cut point. This scenario is likely for FPG and 2-h PG if the glucose samples remain at room temperature and are not centrifuged promptly. Because of the potential for preanalytic variability, it is critical that samples for plasma glucose be spun and separated immediately after they are drawn. If patients have test results near the margins of the diagnostic threshold, the health care professional should follow the patient closely and repeat the test in 3–6 months. Description In 1997 and 2003, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (17,18) recognized a group of individuals whose glucose levels did not meet the criteria for diabetes but were too high to be considered nor- mal. “Prediabetes” is the term used for individuals with IFG and/or IGT and/or A1C 5.7–6.4% (39–47 mmol/mol). Pre- diabetes should not be viewed as a clinical entity in its own right but rather as an increased risk for diabetes (Table 2.3) and cardiovascular disease (CVD). Prediabetes is associated with obesity (especially abdominal or visceral obesity), dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertension. Diagnosis The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (17,18) defined IFG as FPG levels be- tween 100 and 125 mg/dL (between 5.6 and 6.9 mmol/L) and IGT as 2-h PG after 75-gOGTT levels between 140 and 199 mg/dL (between 7.8 and 11.0 mmol/L). It should be noted that the World Health Organization (WHO) and numerous other diabetes organizations define the IFG cutoff at 110 mg/dL (6.1 mmol/L). As with the glucose measures, several prospective studies that used A1C to predict the progression to diabetes as defined by A1C criteria demonstrated a strong, continuous association between A1C and subsequent diabetes. In a systematic review of 44,203 individuals from 16 cohort studies with a follow-up interval averaging 5.6 years (range 2.8– 12 years), those with A1C between 5.5 and 6.0% (between 37 and 42 mmol/mol) had a substantially increased risk of diabetes (5-year incidence from 9 to 25%). An A1C range of 6.0–6.5% (42–48 mmol/mol) had a 5-year risk of developing diabetes between 25 and 50% and a relative risk 20 times higher compared with A1C of 5.0% (31 mmol/mol) (19). In a community- based study of African American and non-Hispanic white adults without diabetes, baseline A1C was a stronger predictor of subsequent diabetes and cardiovascular events than fasting glucose (20). Other analyses suggest that A1C of 5.7% (39 mmol/mol) or higher is associated with a diabetes risk similar to that of the high-risk participants in the Diabetes Prevention Program (DPP) (21), and A1C at baseline was a strong predictor of the development of glucose- defined diabetes during the DPP and its follow-up (22). Hence, it is reasonable to consider an A1C range of 5.7–6.4% (39–47 mmol/mol) as identifying individuals with prediabetes. Similar to those with IFG and/or IGT, individuals with A1C of 5.7–6.4% (39– 47 mmol/mol) should be informed of their increased risk for diabetes and CVD and counseled about effective strategies to lower their risks (see Section 5 “Prevention or Delay of Type 2 Diabetes”). Similar to glucose measurements, the continuum of risk is curvilinear, so as A1C rises, the diabetes risk rises disproportionately (19). Aggressive interventions and vigilant follow-up should be pursued for those considered at very high risk (e.g., those with A1C .6.0% [42 mmol/mol]). · Guideline recommendations to start medications recommendations A complete medical evaluation should be performed at the initial visit to - Confirm the diagnosis and classify diabetes. - Detect diabetes complications and potential comorbid conditions. - Review previous treatment and risk factor control in patients with established diabetes. - Begin patient engagement in the formulation of a care management plan. - Develop a plan for continuing care. Recommendations - Provide routine vaccinations for children and adults with diabetes according to age-related recommendations. C - Annual vaccination against influenza is recommended for all persons with diabetes $6 months of age. - Vaccination against pneumonia is recommended for all people with diabetes 2 through 64 years of age with pneumococcal polysaccharide vaccine (PPSV23). At age $65 years, administer the pneumococcal conjugate vaccine (PCV13) at least 1 year after vaccination with PPSV23, followed by another dose of vaccine PPSV23 at least 1 year after PCV13 and at least 5 years after the last dose of PPSV23. - Administer 3-dose series of hepatitis B vaccine to unvaccinated adults with diabetes who are age 19–59 years. - Consider administering 3-dose series of hepatitis B vaccine to un- vaccinated adults with diabetes who are age $60 years. First line medication options and medication side effectsRecommendations - Metformin, if not contraindicated and if tolerated, is the preferred initial pharmacologic agent for the treatment of type 2 diabetes. - Long-term use of metformin may be associated with biochemical vitamin B12 deficiency, and periodic measurement of vitamin B12 levels should be considered in metformin-treated patients, especially in those with anemia or peripheral neuropathy. B - Consider initiating insulin therapy (with or without additional agents) in patients with newly diagnosed type 2 diabetes who are symptomatic and/or have A1C $10% (86 mmol/mol) and/or blood glucose levels $300 mg/dL (16.7 mmol/L). If noninsulin monotherapy at maximum tolerated dose does not achieve or maintain the A1C target after 3 months, add a second oral agent, a glucagon-like peptide 1 receptor agonist, or basal insulin. - A patient-centered approach should be used to guide the choice of pharmacologic agents. Considerations include efficacy, hypoglycemia risk, impact on weight, potential side ef- fects, cost, and patient preferences. - For patients with type 2 diabetes who are not achieving glycemic goals, insulin therapy should not be delayed. - In patients with long-standing suboptimally controlled type 2 diabetes and established atherosclerotic cardiovascular disease, empagliflozin or liraglutide should be considered as they have been shown to reduce cardiovascular and all-cause mortality when added to standard care. Ongoing studies are investigating the cardio- vascular benefits of other agents in these drug classes. Initial Therapy Metformin monotherapy should be started at diagnosis of type 2 diabetes unless there are contraindications. Metformin is effective and safe, is inexpensive, and may reduce risk of cardiovascular events and death (22). Metformin may be safely used in patients with estimated glomerular filtration rate (eGFR) as low as 30 mL/min/1.73 m2 (23), and the U.S. label for metformin was recently re- vised to reflect its safety in patients with eGFR $30 mL/min/1.73 m2 (24). Patients should be advised to stop the medication in cases of nausea, vomiting, or dehydration. Metformin is associated with vitamin B12 deficiency, with a recent report from the Diabetes Prevention Pro- gram Outcomes Study (DPPOS) suggesting that periodic testing of vitamin B12 levels should be considered in metformin-treated patients, especially in those with anemia or peripheral neuropathy (25). In patients with metformin contraindications or intolerance, consider an initial drug from another class depicted in Fig. 8.1 under “Dual Therapy” and proceed accordingly. When A1C is $9% (75 mmol/mol), consider initiating dual combination therapy (Fig. 8.1) to more expeditiously achieve the target A1C level. Insulin has the advantage of being effective where other agents may not be and should be considered as part of any combination regimen when hyperglycemia is severe, especially if symptoms are pre- sent or any catabolic features (weight loss, ketosis) are present. Consider initiating combination insulin injectable therapy (Fig. 8.2) when blood glucose is $300 mg/dL (16.7 mmol/L) or A1C is $10% (86 mmol/mol) or if the patient has symptoms of hyperglycemia (i.e., polyuria or polydipsia). As the patient’s glucose toxicity resolves, the regimen may, potentially, be simplified. Combination Therapy Although there are numerous trials com- paring dual therapy with metformin alone, ew directly compare drugs as add-on therapy. A comparative effectiveness meta- analysis (23) suggests that each new classof noninsulin agents added to initial therapy generally lowers A1C approximately 0.9–1.1%. If the A1C target is not achieved after approximately 3 months, consider a combination of metformin and one of the six available treatment options: sulfonylurea, thiazolidinedione, DPP-4 inhibitor, SGLT2 inhibitor, GLP- 1 receptor agonist, or basal insulin (Fig. 8.1). If A1C target is still not achieved after ;3 months of dual therapy, proceed to three-drug combination (Fig. 8.1). Again, if A1C target is not achieved after 3 months of triple therapy, proceed to combination injectable therapy (Fig. 8.2). Drug choice is based on patient preferences (26), as well as various patient, disease, and drug characteristics, with the goal of reducing blood glucose levels while minimizing side effects, especially hypoglycemia. Table 8.1 lists drugs commonly used in the U.S. Cost-effectiveness models have suggested that some of the newer agents may be of relatively lower clinical utility based on high cost and moderate glycemic effect (27). Table 8.2 provides cost information for currently approved noninsulin therapies. Of note, prices listed are average wholesale prices (AWP) and do not account for discounts, rebates, or other price adjustments often involved in prescription sales that affect the actual cost incurred by the patient. While there are alternative means to estimate medication prices, AWP was utilized to provide a comparison of list prices with the primary goal of highlighting the importance of cost considerations when pre- scribing antihyperglycemic treatments. The ongoing Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness Study (GRADE) will compare four drug classes (sulfonylurea, DPP-4 inhibitor, GLP-1 receptor agonist, and basal insulin) when added to metformin therapy over 4 years on glycemic control and other medical, psychosocial, and health economic outcomes (28). Rapid-acting secretagogues (meglitinides) may be used instead of sulfonylureas in patients with sulfa allergies, irregular meal schedules, or those who develop late postprandial hypoglycemia when taking a sulfonylurea. Other drugs not shown in Fig. 8.1 (e.g., inhaled insulin, a-glucosidase inhibitors, colesevelam, bromocriptine, and pramlintide) may be tried in specific situations but are not often used due to modest efficacy in type 2 diabetes, the frequency of administration, the potential for drug interactions, and/or side effects. · 2017 HTN guidelines recommended BP ranges for diabetic patients Diabetes mellitus (DM) and hypertension: Antihypertensive drug treatment should be initiated at a BP ≥130/80 mm Hg with a treatment goal of <130/80 mm Hg. In adults with DM and hypertension, all first-line classes of antihypertensive agents (i.e., diuretics, ACE inhibitors, ARBs, and CCBs) are useful and effective. ACE inhibitors or ARBs may be considered in the presence of albuminuria. Subjective signs of hypoglycemia and hyperglycemia ● An irregular heart rhythm ● Fatigue ● Pale skin ● Shakiness ● Anxiety ● Sweating ● Hunger ● Irritability ● Tingling sensation around the mouth● Crying out during sleep ● Confusion, abnormal behavior or both, such as the inability to complete routine tasks ● Visual disturbances, such as blurred vision ● Seizures ● Loss of consciousness Physical signs of elevated glucose you might see on exam ● Increased thirst and/or hunger ● Frequent urination ● Sugar in your urine ● Headache ● Blurred vision ● Fatigue ● High level of ketones in the urine ● Shortness of breath ● Fruit-smelling breath ● Dry mouth Week 6 GU · Incontinence in men and women- common causes and types of incontinence Causes Urinary incontinence (UI), the involuntary loss of urine, has a prevalence of approximately 25% in young women (aged 14 to 21 years) (1), 44% to 57% in middle-aged and postmenopausal women (aged 40 to 60 years) (2), and 75% in elderly women (aged ≥75 years) (3). However, these statistics may be underestimated because one study showed that at least half of incontinent women do not report the issue to their physicians (4). Risk factors for UI include pregnancy, pelvic floor trauma after vaginal delivery, menopause, hysterectomy, obesity, urinary tract infection, functional and/or cognitive impairment, chronic cough, and constipation (5). The effects of UI range from slightly bothersome to debilitating. Urinary incontinence also contributes to high medical spending—approximately $19.5 billion was spent in the United States in 2004—and it accounts for 6% of nursing home admissions for elderly women, costing approximately $3 billion (6). Types – From Harvard Health & Guideline The 2 types of UI are based on the dysfunctional mechanism: stress and urgency. However, the distinction is not always clear, particularly for older women. Stress UI is related to urethral sphincter failure associated with intra-abdominal pressure and results in the inability to retain urine when laughing, coughing, or sneezing (7). Urgency UI is the involuntary loss of urine associated with a sudden and compelling urge to void (7). Mixed UI is a combination of stress and urgency UI. Overactive bladder is a constellation of symptoms that includes urinary urgency (with or without UI), usually accompanied by frequency, and nocturia (5). Stress incontinence If urine leaks out when you jump, cough, or laugh, you may have stress incontinence. Any physical exertion that increases abdominal pressure also puts pressure on the bladder. The word "stress" actually refers to the physical strain associated with leakage. Although it can be emotionally distressing, thecondition has nothing to do with emotion. Often only a small amount of urine leaks out. In more severe cases, the pressure of a full bladder overcomes the body's ability to hold in urine. The leakage occurs even though the bladder muscles are not contracting and you don't feel the urge to urinate. Stress incontinence occurs when the urethral sphincter, the pelvic floor muscles, or both these structures have been weakened or damaged and cannot dependably hold in urine. Stress incontinence is divided into two subtypes. In urethral hypermobility, the bladder and urethra shift downward when abdominal pressure rises, and there is no hammock-like support for the urethra to be compressed against to keep it closed. In intrinsic sphincter deficiency, problems in the urinary sphincter interfere with full closure or allow the sphincter to pop open under pressure. Many experts believe that women who have delivered vaginally are most likely to develop stress incontinence because giving birth has stretched and possibly damaged the pelvic floor muscles and nerves. Generally, the larger the baby, the longer the labor, the older the mother, and the greater the number of births, the more likely that incontinence will result. Age is likewise a factor in stress incontinence. As a woman gets older, the muscles in her pelvic floor and urethra weaken, and it takes less pressure for the urethra to open and allow leakage. Estrogen can also play some role, although it is not clear how much. Many women do not experience symptoms until after menopause. Overactive bladder (urge incontinence) If you feel a strong urge to urinate even when your bladder isn't full, your incontinence might be related to overactive bladder, sometimes called urge incontinence. This condition occurs in both men and women and involves an overwhelming urge to urinate immediately, frequently followed by loss of urine before you can reach a bathroom. Even if you never have an accident, urgency and urinary frequency can interfere with work and a social life because of the need to keep running to the bathroom. Urgency is caused when the bladder muscle, the detrusor, begins to contract and signals a need to urinate, even when the bladder is not full. Another name for this phenomenon is detrusor overactivity. Overactive bladder can result from physical problems that keep your body from halting involuntary bladder muscle contractions. Such problems include damage to the brain, the spine, or the nerves extending from the spine to the bladder — for example, from an accident, diabetes, or neurological disease. Irritating substances within the bladder, such as those produced during an infection, might also cause the bladder muscle to contract. Often there is no identifiable cause for overactive bladder, but people are more likely to develop the problem as they age. Postmenopausal women, in particular, tend to develop this condition, perhaps because of age-related changes in the bladder lining and muscle. African American women with incontinence are more likely to report symptoms of overactive bladder than stress incontinence, while the reverse is true in white women. A condition called myofascial pelvic pain syndrome has been identified with symptoms that include overactive bladder accompanied by pain in the pelvic area or a sense of aching, heaviness, or burning. In addition, infections of the urinary tract, bladder, or prostate can cause temporary urgency. Partial blockage of the urinary tract by a bladder stone, a tumor (rarely), or, in men, an enlarged prostate (a condition known as benign prostatic hyperplasia, or BPH) can cause urgency, frequency, and sometimesurge incontinence. Surgery for prostate cancer or BPH can trigger symptoms of overactive bladder, as can freezing (cryotherapy) and radiation seed treatment (brachytherapy) for prostate cancer. Neurological diseases (such as Parkinson's disease and multiple sclerosis) can also result in urge incontinence, as can a stroke. When hospitalized following a stroke, 40% to 60% of patients have incontinence; by the time they are discharged, 25% still have it, and one year later, 15% do. Overflow incontinence If your bladder never completely empties, you might experience urine leakage, with or without feeling a need to go. Overflow incontinence occurs when something blocks urine from flowing normally out of the bladder, as in the case of prostate enlargement that partially closes off the urethra. It can also occur in both men and women if the bladder muscle becomes underactive (the opposite of an overactive bladder) so you don't feel an urge to urinate. Eventually the bladder becomes overfilled, or distended, pulling the urethra open and allowing urine to leak out. The bladder might also spasm at random times, causing leakage. This condition is sometimes related to diabetes or cardiovascular disease. Men are much more frequently diagnosed with overflow incontinence than women because it is often caused by prostate-related conditions. In addition to enlarged prostate, other possible causes of urine blockage include tumors, bladder stones, or scar tissue. If a woman has severe prolapse of her uterus or bladder (meaning that the organ has dropped out of its proper position), her urethra can become kinked like a bent garden hose, interfering with the flow of urine. Nerve damage (from injuries, childbirth, past surgeries, or diseases such as diabetes, multiple sclerosis, or shingles) and aging often prevent the bladder muscle from contracting normally. Medications that prevent bladder muscle contraction or that make you unaware of the urge to urinate can also result in overflow incontinence. Functional incontinence If your urinary tract is functioning properly but other illnesses or disabilities are preventing you from staying dry, you might have what is known as functional incontinence. For example, if an illness rendered you unaware or unconcerned about the need to find a toilet, you would become incontinent. Medications, dementia, or mental illness can decrease awareness of the need to find a toilet. Even if your urinary system is fine, it can be extremely difficult for you to avoid accidents if you have trouble getting to a toilet. This problem can affect anyone with a condition that makes it excessively difficult to move to the bathroom and undress in time. This includes problems as diverse as having arthritis, being hospitalized or restrained, or having a toilet located too far away. If a medication (such as a diuretic used to treat high blood pressure or heart failure) causes you to produce abnormally large amounts of urine, you could develop incontinence that requires a change in treatment. If you make most of your urine at night, the result might be nocturnal incontinence, or bedwetting. Reflex incontinence Reflex incontinence occurs when the bladder muscle contracts and urine leaks (often in large amounts) without any warning or urge. This can happen as a result of damage to the nerves that normally warn the brain that the bladder is filling. Reflex incontinence usually appears in people with serious neurologicalimpairment from multiple sclerosis, spinal cord injury, other injuries, or damage from surgery or radiation treatment · Diagnoses which present as urinary difficulty in men Type of Problem Etiology Treatment Pyelonephritis Cystitis Coliform organisms Coliform organisms Urethritis Neisseria gonorrhoeae, Chlamydia trachomatis Prostatitis Epididymoorchit is Coliform organisms Coliform organisms, viruses (e.g., mumps virus) Meatitis and urethritis Obstruction Benign prostatic hyperplasia Urethral stricture Malignancy Renal cell tumor Unknown Surgery, chemotherapy Age and androgens Alpha blockers, finasteride (Proscar), hyperthermia therapy, surgery Previous surgery Dilation, surgery Herpes simplex virus II Quinolones; aminoglycosides plus ampicillin (Principen); third-generation cephalosporins; piperacillin (Pipracil) Trimethoprim-sulfamethoxazole (Bactrim), quinolones, cephalosporins, nitrofurantoin (Furadantin), amoxicillin (Amoxil) Ceftriaxone (Rocephin) plus doxycycline (Vibramycin); macrolides; quinolones Quinolones, doxycycline, trimethoprim-sulfamethoxazole Quinolones, doxycycline, trimethoprim-sulfamethoxazole Acyclovir (Zovirax), famciclovir (Famvir), valacyclovir (Valtrex)Bladder cancer Smoking, aniline dye exposure Stone disease Metabolic disorders, infection Spondyloarthropathy Behçet's syndrome Reiter's syndrome Toxicity or drug side effects Unknown Unknown Dopamine, cantharidin and others Anti-inflammatory drugs, immunosuppressants Anti-inflammatory drugs, immunosuppressants Avoidance Surgery, radiation therapy, chemotherapy Hydration, pain management, antibiotics (if infection is present), correction of metabolic defects (e.g., allopurinol [Zyloprim] for hyperuricemia) *—Exact treatment varies, depending on patient and antibiotic sensitivities. · BPH: diagnosis testing, common medications (including most common side effects) and recommended follow up Diagnosis Diagnosis of BPH often rules out other clinical manifestations that may present with similar symptoms. Examples include prostate cancer, prostatitis, bladder cancer, bladder stones, overactive bladder (OAB), interstitial cystitis, and urinary tract infections; all of which may also cause LUTS.3 Although symptoms related to BPH are often not life-threatening, they can be debilitating and affect quality of life (QOL) significantly. Thus, it is important to identify and correctly diagnose BPH in order to pursue an effective treatment strategy. The American Urological Association (AUA) guideline panel made several recommendations for the diagnosis of BPH that were consistent with an article published by Abrams et al in 2009.2,4 The recommendations state that a basic evaluation should be performed on patients who are experiencing negative changes in their QOL due to LUTS. This evaluation may include several components, which are summarized in FIGURE 1. If the initial evaluation shows the presence of LUTS associated with one or more of the digital rectal examination (DRE) findings suspicious of prostate cancer, hematuria, abnormal prostate-specific antigen (PSA), pain, recurrent infection (infection should be assessed before referral), palpable bladder, or neurologic disease, the patient should be referred to a urologist for additional evaluation before pursuing treatment. Medications If lifestyle modifications are insufficient in improving QOL, then pharmacotherapy may be indicated in patients who do not have absolute indications warranting surgery.5 Current oral pharmacotherapy options for managing BPH include: alpha-adrenergic antagonists (alpha-blockers: - Alfuzosin (Uroxatral), Doxazosin (Cardura), Tamsulosin (Flomax, Terazosin (Hytrin), Silodosin (Rapaflo),- 5-alpha-reductase inhibitors (5ARIs): Dutasteride (Avodart), Finasteride (Proscar) - muscarinic receptor antagonists (MRAs): Tolterodine (Detrol), Tolerodine (Detrol LA), Festerodine (Toviaz) - phosphodiesterase 5 (PDE5) inhibitors: Tadalafil (Cialis) - Anticholinergics - Combination therapy Follow up Watchful waiting is appropriate in patients who do not need surgery. Side Effects Alpha blockers – ED, abnormal ejaculation, dizziness, HA, orthostatic hypotension, fatigue, infection, QT interval prolongation, polydipsia, IFIS 55AR’s – Libido impairment, abnormal ejaculation, erectile dysfunction, mastalgia, gynecomastia MRA’s – Xerostomia (dry mouth) PDE5 inhibitors – Back pain, dyspepsia, flushing, myalgia, nausea, pharyngitis, nausea, pharyngitis · Prostatitis signs & symptoms, assessment and treatment Signs & Symptoms Prostatitis signs and symptoms depend on the cause. They can include: [Show More]

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